Thus a better understanding of the molecular basis of apoptotic cell degradation could be of key importance to multiple aspects of normal cellular homeostasis and disease.
WASP is key in transducing signals from the cell surface to the actin cytoskeleton, and a lack of WASp results in cytoskeletal defects that compromise multiple aspects of normal cellular activity including proliferation, phagocytosis, immune synapse formation, adhesion and directed migration.
The tumor suppressor p53 is one of the most studied and most important regulators of multiple signaling pathways, including normal cellular processes and those triggered by diverse cellular stresses.
The wealth of Ras activators and effectors identified in mammalian cells places the Ras proteins at the center of multiple signaling networks critical for normal cellular development and homeostasis and for pathological processes such as cancer [ 1- 4, 7- 9].
The ER has vital roles in multiple processes that are required for normal cellular function, including the synthesis and processing of proteins and lipids, regulation of glucose and calcium homeostasis, and metabolism of xenobiotic compounds (1, 3).
A component of this invariant expression is produced by a subset of the genome comprising "housekeeping genes" that are continuously and ubiquitously expressed across multiple tissues and are likely essential for normal cellular function[18] [21].
Cancer cells display multiple defects in cellular pathways that govern normal cellular proliferation and homeostasis.
The ER is an organelle that has essential roles in multiple cellular processes required for cell survival and normal cellular functions.
As a result, the mammalian cell death machinery is intertwined with multiple cellular signaling processes that are part of normal cellular physiological signaling processes, providing backups and flexible signaling mechanisms to cell death signaling.
Increased ERBB2/3 alters multiple signaling pathways, including kinase signaling, and, thus, impairs normal cellular control mechanisms, giving rise to malignant tumor cell transformation [ 42].
